Chapter 23: Oral Complications in Diabetes

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Chapter 23 Oral Complications in Diabetes

Harald Löe, DDS, and Robert J. Genco, DDS, PhD

SUMMARY

ata regarding oral complications in diabe- ated with altered phagocyte functions and reduced tes prior to the insulin era are scarce, pos- healing capacity associated with altered collagen me- sibly due to the limited scope of oral health tabolism may explain, in part, the increased levels of care of that time and the short life span of periodontal disease in diabetes. Dthe insulin-requiring diabetic patient. During the past 40 years, much data have been generated emphasizing Caries in the crowns of teeth appear to be greater in the frequent occurrence of oral afflictions in patients adults with poor control of IDDM. However, the with insulin-dependent diabetes mellitus (IDDM) and prevalence of root caries requires further studies. Oral non-insulin-dependent diabetes mellitus (NIDDM). infections aside from dental caries and periodontal Perhaps the most important finding is that periodon- disease are often more severe. Life-threatening deep tal disease is more severe and occurs with higher neck infections and palatal ulcers exemplify the sever- frequency in diabetic patients (both NIDDM and ity of these conditions. Mucosal abnormalities and IDDM), especially if the diabetes is not well controlled oral bacterial and fungal infections may reflect undi- and there are other complications, such as reti- agnosed diabetes or identify poorly controlled diabe- nopathy. The reason for the greater occurrence of tes. Successful management of oral infections, includ- periodontal destruction in diabetes is not clear. How- ing periodontal diseases, seems to depend on estab- ever, studies of the periodontal flora find similar mi- lishing metabolic control in diabetic patients. Knowl- croorganisms in diabetic and nondiabetic individuals, edge of oral co-morbidity among people with diabetes suggesting that alteration in host responses to peri- is generally poor and suggests the need for appropri- odontal pathogens account for these differences in ate health education and health promotion to improve periodontal destruction. For example, increased sus- the oral health of diabetic patients. ceptibility to infection by periodontal bacteria associ-

• • • • • • •

CARIES (TOOTH DECAY) PERIODONTAL DISEASE

Children with IDDM have been reported to have car- Periodontal disease is the most prevalent oral compli- ies incidence that is higher1, lower2-4, or similar to that cation in IDDM and NIDDM patients and has been of nondiabetic children. This contradiction may pos- labeled the "sixth complication of diabetes melli- sibly be explained by cohort characteristics, degree of tus"10. Numerous studies have shown both increased diabetes control, and degree of adherence to dietary prevalence and severity of periodontal disease in pa- prescriptions. Adult patients with poor control of tients with IDDM. Diabetic children and adults with their IDDM seem to have more coronal caries5-7. In the less than optimal metabolic control show a tendency general population, the frequency of root caries in- towards higher gingivitis scores11-17. Early case reports creases with age and is three times more prevalent in suggested that diabetic adolescents and teenagers may those age ≥65 years compared with young adults8. suffer from periodontitis18. In a more recent study, the However, very few studies have reported on the inci- prevalence of periodontal disease was 9.8% in 263 dence of root-surface caries as a significant problem in patients with IDDM, compared with 1.7% in people older patients with IDDM or NIDDM9. without diabetes19. Most of the periodontal disease was found in those age 11-18 years (Figure 23.1).

501 Figure 23.1 Figure 23.3 Prevalence of Periodontal Disease in IDDM Patients, Periodontal Attachment Loss According to Retinal by Age Changes in IDDM Patients and Nondiabetic Persons

100 Gingivitis Periodontitis 98 4.0

77 77 80 74 66 3.0 61 60

40 2.0 30

20 15.5 15.1 9 4.2 1.0 0 0 #10 11-12 13-14 15-16 17-18$ 19 Age (Years) 0.0 Nondiabetic IDDM, No IDDM, Retinal Changes Retinal Changes Source: Reference 19

However, earlier rapid periodontal destruction was Source: Reference 21 not found in adolescent patients with IDDM in Fin- land15. This difference may be related to different lev- the loss of periodontal attachment is significantly els of metabolic control in participants of the two larger than in IDDM patients without retinal changes studies. For example, case reports suggest a strong (Figure 23.3). relationship between rapid periodontal breakdown and elevated blood glucose levels20. Several studies have clearly demonstrated that IDDM patients with poor long-term control of diabetes have Patients with IDDM of >10 years duration had greater increased extent and severity of periodontal disease, loss of periodontal attachment compared with those whereas those who maintain good metabolic control of <10 years duration21. This was found to be particu- have minimal periodontal problems. Patients with larly true for patients age ≥35 years (Figure 23.2). IDDM of long duration who have retinopathy tend to More recently, it was reported that IDDM patients age exhibit more loss of periodontal attachment as they 40-50 years with long IDDM duration had signifi- reach age 40-50 years. Good oral home care and fre- cantly more sites with advanced periodontal destruc- quent professional check-ups and care are important tion and alveolar bone loss than people without dia- for these patients22. betes17. It has also been demonstrated21 and con- firmed16 that in IDDM patients with retinal changes Few studies have dealt with NIDDM subjects. In a

Figure 23.2 Figure 23.4 Periodontal Attachment Loss in IDDM Patients and Severity of Periodontal Disease Among Diabetic and Nondiabetic Persons Nondiabetic Pima Indians

5 Diabetic Nondiabetic 5.0 Nondiabetic IDDM 4

4.0 3 3.0 2 2.0

1.0 1

0.0 0 20-30 30-40 15-24 25-34 35-44 45-54 Age (Years) Age (Years)

Source: Reference 21 Source: Reference 23

502 study of Pima Indians, 40% of whom have NIDDM, NIDDM had no teeth. The odds ratio for subjects with diabetic patients age <40 years had increased attach- NIDDM for increased risk of periodontal destruction ment loss, and alveolar bone loss was associated with was 3.43 (95% confidence interval (CI) 2.28-5.16)24. increased glucose intolerance23. Periodontal tissue In this population, the age- and sex-adjusted inci- loss increased with age and was higher in people with dence of periodontal disease in subjects with NIDDM diabetes compared with people without diabetes in all was 75 cases per 1,000 person-years, which was sub- age groups (Figure 23.4). Alveolar bone loss also in- stantially higher than the rate of 29 cases per 1,000 creased with age and was substantially more frequent person-years in subjects without diabetes25 (Table 23.1). in patients with NIDDM compared with nondiabetic people age 5-44 years (Figure 23.5). Toothlessness Early studies of the pathogenesis of periodontal dis- was 15 times higher in the diabetic than in the nondi- ease in diabetic patients centered on the general fea- abetic group. Indeed, 30% of these young adults with ture of "basement membrane thickening"26 and possi-

Figure 23.5 Distribution of Interproximal Alveolar Bone Loss in Diabetic and Nondiabetic Persons

Nondiabetic Subjects Diabetic Subjects 100 100 17 16 15 14 13 12 1121 22 23 24 25 26 27 17 16 15 14 13 12 1121 22 23 24 25 26 27 80 80 60 60 40 40 20 20 0 0 -2020 -2020 -4040 -4040 -6060 -6060 -8080 -8080 -100100 -100100 47 46 45 44 43 42 41 31 32 33 34 35 36 37 47 46 45 44 43 42 41 31 32 33 34 35 36 37 Tooth Number Tooth Number

Bone loss is expressed as percent of individuals who have teeth affected by ≥25% bone loss as determined by measurements from panoramic radiographs. The 2-digit tooth numbers are: first digit refers to the quadrant (1, upper right; 2, upper left; 3, lower left; 4, lower right); second digit refers to tooth type (7 and 6 are molars; 5 and 4 are premolars; 3 is a canine; 2 and 1 are incisors).

Source: Reference 23

503 Table 23.1 ments may be due to a low degree of mumps infection 44 ++ Incidence of Periodontal Disease in Pima Indians by has been mentioned . Increased concentration of Ca Diabetes Status in both parotid and submandibular saliva of IDDM subjects45 might explain the frequently reported in- Age- and sex-adjusted incidence crease in calculus formation in such patients. How- Diabetes status (new cases/1,000 person-years) ever, in well-controlled individuals with altered glu- Nondiabetic 28.9 cose metabolism, salivary gland function does not NIDDM 75.5 seem to be significantly impaired46. Relative risk 2.6

Source: Reference 25 OTHER PATHOLOGICAL FEATURES OF THE ORAL CAVITY ble changes in the vasculature27-29. More recent studies have focused on the role of the periodontal infection15, the microflora of dental plaque30, collagen metabo- Other pathology associated with diabetes includes lism31,32, leukocyte function33, and other aspects of the oral infections other than those responsible for dental host response34,35. All of these factors may individually caries and periodontal destruction. Case reports on or synergistally contribute to periodontal disease. life-threatening deep neck infection from a periodontal abscess47 and fatal palatal ulcers48 exemplify the The reason for the greater occurrence of periodontal severity of these conditions. To what extent such inci- destruction in diabetics is not clear. However, studies dents are part of the broader issue of increased occur- of the periodontal flora find similar microorganisms rence of infection in people with diabetes, or may have in diabetic and nondiabetic people30,36, suggesting that strictly a local etiology, is open to question. In addi- alteration in host responses to periodontal pathogens tion to these infections, other localized or regional account for these differences in periodontal destruc- infections such as mucormycosis, "malignant otitis tion. For example, increased susceptibility to infec- media," necrotizing cellulitis, urinary tract infections, tion by periodontal bacteria associated with altered skin infections, and pneumonia have also been found phagocyte functions and reduced healing capacity as- more often in poorly controlled diabetic patients than sociated with altered collagen metabolism may ex- in others. There are also indications that patients with plain, in part, the increased levels of periodontal dis- elevated salivary glucose levels carry candida in- ease in diabetic patients. traorally more often than those with lower glucose levels49. Moreover, a study of 40 patients with lichen The response to treatment suggests that the periodon- planus found that 11 patients (28%) had overt or tal lesions are eminently treatable37,38 and that eradica- latent diabetes, compared with none of the control tion of the infection and the inflammatory foci may group50, the implication being that diabetes may be reduce insulin requirements39. The knowledge among related to the pathogenesis of lichen planus. The evi- people with diabetes of oral co-morbidity is generally dence for an immunological defect51 and deficient poor40 and suggests the need for appropriate health leukocyte functions superimposed on the metabolic education and health promotion to improve the oral abnormality of diabetes seems increasingly convincing. health of diabetic patients. Finally, it should be mentioned that diabetes may initially manifest with oral symptoms other than SALIVA thirst52. Mucosal abnormalities, such as erosive lichen planus, burning tongue, and gingival bleeding, as well as sialorrhoea and sialosis, have been found in undi- Reduced salivary secretion has been a frequent finding agnosed NIDDM, most of which resolved on treat- in experimental diabetes in animals41 as well as in ment directed at improving glycemic control52. IDDM patients. A non-inflammatory, non-neoplastic enlargement of the parotid gland is believed to occur in 25% of patients with moderate to severe diabetes Dr. Harald Löe is Former Director, National Institute of Den- and especially in IDDM patients with poor metabolic tal Research, National Institutes of Health, Bethesda, MD and control42. The etiology of this condition is unknown, University Professor, Department of Periodontology, Univer- but it is speculated that the enlargement occurs in sity of Connecticut Dental School, Farmington, CT; Dr. response to decreased insulin production or that the Robert J. Genco, is Distinguished Professor and Chair, De- Sjögren’s syndrome may underlie this symptom43. partment of Oral Biology, School of Dentistry, State Univer- Also, the possibility that in some cases these enlarge- sity of New York, Buffalo, NY.

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